Topological localization in out-of-equilibrium dissipative systems

In this paper we report that notions of topological protection can be applied to stationary configurations that are driven far from equilibrium by active, dissipative processes. We show this for physically two disparate cases : stochastic networks governed by microscopic single particle dynamics as well as collections of driven, interacting particles described by coarse-grained hydrodynamic theory. In both cases, the presence of dissipative couplings to the environment that break time reversal symmetry are crucial to ensuring topologically protection. These examples constitute proof of principle that notions of topological protection, established in the context of electronic and mechanical systems, do indeed extend generically to processes that operate out of equilibrium. Such topologically robust boundary modes have implications for both biological and synthetic systems.Comment: 11 pages, 4 figures (SI: 8 pages 3 figures

Liquid behavior of cross-linked actin bundles

The actin cytoskeleton is a critical regulator of cytoplasmic architecture and mechanics, essential in a myriad of physiological processes. Here we demonstrate a liquid phase of actin filaments in the presence of the physiological cross-linker, filamin. Filamin condenses short actin filaments into spindle-shaped droplets, or tactoids, with shape dynamics consistent with a continuum model of anisotropic liquids. We find that cross-linker density controls the droplet shape and deformation timescales, consistent with a variable interfacial tension and viscosity. Near the liquid-solid transition, cross-linked actin bundles show behaviors reminiscent of fluid threads, including capillary instabilities and contraction. These data reveal a liquid droplet phase of actin, demixed from the surrounding solution and dominated by interfacial tension. These results suggest a mechanism to control organization, morphology, and dynamics of the actin cytoskeleton

Bound states of edge dislocations: The quantum dipole problem in two dimensions

We investigate bound state solutions of the 2D Schr\"odinger equation with a dipole potential originating from the elastic effects of a single edge dislocation. The knowledge of these states could be useful for understanding a wide variety of physical systems, including superfluid behavior along dislocations in solid $^4$He. We present a review of the results obtained by previous workers together with an improved variational estimate of the ground state energy. We then numerically solve the eigenvalue problem and calculate the energy spectrum. In our dimensionless units, we find a ground state energy of -0.139, which is lower than any previous estimate. We also make successful contact with the behavior of the energy spectrum as derived from semiclassical considerations.Comment: 6 pages, 3 figures, submitted to PR

Dislocation-induced superfluidity in a model supersolid

Motivated by recent experiments on the supersolid behavior of $^4$He, we study the effect of an edge dislocation in promoting superfluidity in a Bose crystal. Using Landau theory, we couple the elastic strain field of the dislocation to the superfluid density, and use a linear analysis to show that superfluidity nucleates on the dislocation before occurring in the bulk of the solid. Moving beyond the linear analysis, we develop a systematic perturbation theory in the weakly nonlinear regime, and use this method to integrate out transverse degrees of freedom and derive a one-dimensional Landau equation for the superfluid order parameter. We then extend our analysis to a network of dislocation lines, and derive an XY model for the dislocation network by integrating over fluctuations in the order parameter. Our results show that the ordering temperature for the network has a sensitive dependence on the dislocation density, consistent with numerous experiments that find a clear connection between the sample quality and the supersolid response.Comment: 10 pages, 6 figure

Apolipoproteins AI/B/E gene polymorphism and their plasma levels in patients with coronary artery disease in a tertiary care-center of Eastern India

Aim: The present study was designed to investigate whether the three-apolipoprotein (AI, B, E) gene polymorphisms were related to alter their plasma protein levels and hence associated to coronary artery disease (CAD). Methods: We determined distribution of MspI apo AI, EcoRI apo B, HhaI apo E gene polymorphisms, plasma apolipoproteins and lipids levels among 150 patients having CAD admitted to the Department of Cardiology, N.R.S. Medical College & Hospital, Kolkata, India during June 2010–June 2012 and 150 age sex matched healthy controls. Results: We found that ApoAI concentration of studied population was significantly different in each genotypes of −75 G/A apo AI (p < 0.0001) gene polymorphism. A significant association was found in multivariate analysis for the genotypes with apo E4 allele [odds ratio (OR): 3.639; 95% confidence interval (CI): 1.019–12.995, p = 0.040] with four conventional risk factors (i.e. smoking, low-density lipoprotein, ApoAI and ApoB) with CAD. In contrast E2 allele has reverse effect, but the genotypes with apo E2 allele was no longer significant in the multivariate model (OR: 1.788; 95% CI: 0.400–8.001, p = 0.447) where as being significant in univariate analysis (OR: 0.219; 95% CI: 0.087–0.552, p = 0.001). Conclusions: Our findings suggest that the polymorphisms apo AI MspI and apo B EcoRI do not seem to affect CAD. But the genotype with E4 allele of apo E gene independent of other risk factors is associated with this disease

Clots reveal anomalous elastic behavior of fiber networks

The adaptive mechanical properties of soft and fibrous biological materials are relevant to their functionality. The emergence of the macroscopic response of these materials to external stress and intrinsic cell traction from local deformations of their structural components is not well understood. Here, we investigate the nonlinear elastic behavior of blood clots by combining microscopy, rheology, and an elastic network model that incorporates the stretching, bending, and buckling of constituent fibrin fibers. By inhibiting fibrin cross-linking in blood clots, we observe an anomalous softening regime in the macroscopic shear response as well as a reduction in platelet-induced clot contractility. Our model explains these observations from two independent macroscopic measurements in a unified manner, through a single mechanical parameter, the bending stiffness of individual fibers. Supported by experimental evidence, our mechanics-based model provides a framework for predicting and comprehending the nonlinear elastic behavior of blood clots and other active biopolymer networks in general